Key result
Higher CRP correlates with an amplified impact of LVDs on plasma BNP levels.
Why the study?
Does low-grade inflammation (measured by CRP) influence plasma BNP levels in patients with cardiovascular diseases?
Cross-Sectional (n=417)
No
Does low-grade inflammation (measured by CRP) influence plasma BNP levels in patients with cardiovascular diseases?
Effect estimate: β-coefficient 9.406 (95% CI 7.367-11.445)
p-value: p=<0.001
Plasma BNP levels are influenced not only by cardiac dysfunction but also by systemic inflammation (CRP), suggesting BNP is a collective marker for life-threatening conditions.
CRP may confound BNP as a pure hemodynamic marker in CV patients; leaves open whether inflammation-adjusted thresholds improve risk stratification.
OBJECTIVE: B-type natriuretic peptide (BNP) is a cardiac hormone. The results of previous in vitro studies suggest that neurohumoral factors, and not only hemodynamic factors, may cause BNP secretion. In this study, we examined the impact of serum C-reactive protein (CRP) levels on the relationship between echocardiographic parameters and plasma BNP levels in patients with cardiovascular diseases. METHODS AND PATIENTS: The study population comprised 417 patients who visited our cardiovascular unit with a problem. Both blood sampling and echocardiography were performed within one month. RESULTS: Multiple regression analysis showed that plasma BNP levels were negatively correlated with male gender, body mass index, and estimated glomerular filtration rate, and positively correlated with serum CRP levels and left ventricular end-systolic dimension (LVDs). The study population was divided into two groups based on the 75th percentile of the serum CRP levels. Single regression analysis showed that a regression line between LVDs and plasma BNP levels was steeper in the group of patients with CRP levels above the 75th percentile. Multiple regression analysis revealed that the interaction term (LVDs×CRP) was significant, which means LVDs had more impact on plasma BNP levels at higher CRP levels. CONCLUSION: Plasma BNP levels increased with respect to the severity of cardiac dysfunction and serum CRP levels, and should therefore be considered a collective or total marker for life-threatening conditions including systemic inflammation, and not simply as a marker of cardiac dysfunction in patients with cardiovascular diseases.
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Inoue et al. (2010) conducted a cross-sectional in Cardiovascular diseases (n=417). Serum C-reactive protein (CRP) levels vs. Lower CRP levels was evaluated on Plasma BNP levels (interaction between LVDs and CRP) (β-coefficient 9.406, 95% CI 7.367-11.445, p=<0.001). Higher serum C-reactive protein levels significantly amplified the impact of left ventricular end-systolic dimension on plasma B-type natriuretic peptide levels (interaction β=9.406, p<0.001).
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